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Long non-coding RNA MEG3 promotes angiogenesis by directly regulating integrin signaling impairing endothelial cell function

ABSTRACT: We depleted MEG3-lncRNA using GapmeRs in primary human ECs. Total MEG3-regulated targets were obtained.

ORGANISM(S): Homo sapiens

PROVIDER: GSE253830 | GEO | 2024/04/12

REPOSITORIES: GEO

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Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIP-seq]

Project description:We immunoprecipitated EZH2, together with associated chromatin isolated from the HUVECs (2 x 10^6) that were transfected with MEG3 GapmeRs (10 nM, 48 h) or a scrambled control GapmeRs (Ctr). For transfection, we used 10 nM scrambled LNA (locked nucleic acids) GapmeR control (Cat. No. 339515) or phosphorothioate antisense standard GapmeRs MEG3-lncRNA (Cat No. 339511, Qiagen). On beads crosslinked chromatin complexes were reversed, and DNA purified using QIAquick® PCR Purification Kit and quantified by Qubit HS assay (Q33230)

2024-04-12 | GSE234543 | GEO

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function [ChIRP-seq]

Project description:We profiled MEG-DNA interactions using gluteraldehyde assisted chromatin immunoprecipitation by RNA purification (ChIRP-seq) in primary human ECs. Genome-wide MEG3-associated loci were obtained.

2024-04-12 | GSE234542 | GEO

Long Non-Coding RNA MEG3 Promotes Angiogenesis by directly regulating integrin signaling impairing endothelial cell function.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-12 | GSE234544 | GEO

ChIP-seq in MEG3+ and MEG3- hIPSCs

Project description:In this experiment we sought to identify region with differential PRC2, JARID2, and H3K27me3 occupancy in human induced pluripotent stem cell lines with silenced or expressed MEG3 locus to indirectly determine the effect of this ncRNA on PRC2 function. 8 hIPSC lines, 5 MEG3+ and 3 MEG3-; ChIP-seq for EZH2, JARID2, and H3K27me3. Some done in replicates.

2013-12-25 | E-GEOD-48516 | biostudies-arrayexpress

Histone H3K27 methyltransferase EZH2 interacts with MEG3-lncRNA to directly regulate integrin signaling and endothelial cell function

Project description:We profiled EZH2-RNA interactions using formaldehyde/UV assisted cross-linking ligation and sequencing of hybrids (FLASH-seq) in primary human ECs. Transcriptome-wide EZH2-associated ncRNAs and RNA–RNA interactome were obtained.

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The long non-coding RNA Meg3 mediates imprinted gene expression during stem cell differentiation

Project description:The imprinted Dlk1-Dio3 domain comprises the developmental genes Dlk1 and Rtl1, which are silenced on the maternal chromosome in different cell types. On this parental chromosome, the domain’s imprinting control region activates a polycistron that produces the lncRNA Meg3 and many miRNAs (Mirg) and C/D-box snoRNAs (Rian). Although Meg3 lncRNA is nuclear and associates with the maternal chromosome, it is unknown whether it controls gene repression in cis. We created mouse embryonic stem cells (mESCs) that carry an ectopic poly(A) signal, reducing RNA levels along the polycistron, and generated Rian-/- mESCs as well. Upon ESC differentiation, we found that Meg3 lncRNA (but not Rian) is required for Dlk1 repression on the maternal chromosome. Biallelic Meg3 expression acquired through CRISPR-mediated demethylation of the paternal Meg3 promoter led to biallelic Dlk1 repression, and to loss of Rtl1 expression. lncRNA expression also correlated with DNA hypomethylation and CTCF binding at the 5’-side of Meg3. Using Capture Hi-C, we found that this creates a Topologically Associating Domain (TAD) organization that brings Meg3 close to Dlk1 on the maternal chromosome. The requirement of Meg3 for gene repression and TAD structure may explain how aberrant MEG3 expression at the human DLK1-DIO3 locus associates with imprinting disorders.

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Meg3 non-coding RNA expression controls imprinting by preventing transcriptional up-regulation in cis

Project description:Although many long non-coding RNAs (lncRNAs) are controlled by genomic imprinting, their roles often remain unknown. The Dlk1-Dio3 imprinted domain expresses the lncRNA Meg3 (also called Gtl2) and multiple microRNAs and snoRNAs from the maternal chromosome. This locus constitutes an epigenetic model for pluripotency and development, particularly for neurogenesis. The domain’s Dlk1 (Delta-like-1) gene encodes a ligand that inhibits Notch1 signalling and regulates diverse developmental processes. Using a hybrid embryonic stem (ES) cell system, we find that Dlk1 becomes imprinted during neural differentiation and that this involves chromatin activation and transcriptional up-regulation on the paternal chromosome. On the maternal chromosome, the Dlk1 gene remains poised. This allelic protection against gene activation is controlled in cis by Meg3 expression and also involves the H3-lysine-27 methyltransferase Ezh2. Maternal Meg3 expression additionally protects against de novo DNA methylation at its promoter. Concordantly, we find that the lncRNA Meg3 is nuclear, accumulates onto the imprinted locus and overlaps in cis with Dlk1 in embryonic cells. Our data evoke an imprinting model in which a mono-allelic lncRNA prevents chromatin and gene activation in cis during development.

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overexpression/knockdown MEG3 in C2C12 cell lines

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2018-09-28 | GSE73524 | GEO

Herbaspirillum sp. meg3

Project description:Herbaspirillum sp. meg3 Genome sequencing

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Meg3 regulated genes in pancreatic beta cells

Project description:Meg3 is a long non-coding RNA. It's target genes are unknown. The mouse pancreatic beta cell line MIN6-4N was used to assess the expression of genes upon stable Meg3 overexpression Stable cell lines were isolated that have integated pcDNA3.1 or pcDNA3.1-mMeg3.The cells were processed for RNA isolation. The level of Meg3 expression was assessed by RT-PCR. RNA preps were used for microarray analysis.

2015-05-21 | E-GEOD-57716 | biostudies-arrayexpress

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